By way of definition, the term "tachyarrhythmia" refers to any fast, abnormal rhythm of a heart chamber which may be amenable of conversion to a normal sinus rhythm by "cardioversion" or "defibrillation" or the application of certain anti-tachycardia pacing therapies to the heart chamber. Such tachyarrhythmias include ventricular tachycardia (VT), supraventricular tachycardia (SVT), ventricular flutter or fibrillation (VF), atrial tachycardia (AT), and atrial flutter or fibrillation (AF).
In the field of automatic implantable arrhythmia control devices, particularly ICDs (also referred to as pacemaker/cardioverter/defibrillators or PCDs), the terms "cardioversion" or "cardioverter" and "defibrillation" and "defibrillator" generally refer to the processes of and devices for discharging relatively high energy electrical shocks into or across cardiac tissue to arrest a life threatening tachyarrhythmia. In practice, the conversion of AT or VT or low rate AF or VF to normal sinus rhythm by a relatively low amplitude cardioversion shock delivered in timed synchrony with a sensed atrial or ventricular cardiac depolarization (P-wave or R-wave) is typically referred to as "cardioversion". The conversion of malignant AF or VF by the same or higher energy shock delivered without such synchronization is typically referred to as "defibrillation".
Implantable cardiac pacing functions are also currently incorporated into ICDs to supplant some or all of an abnormal heart's natural pacing function by delivering appropriately timed electrical pacing pulses to cause the chamber or chambers of the heart to contract or "beat", i.e., to "capture" the heart. Either single chamber (atrial or ventricular) pacing functions or dual chamber (atrial and ventricular) pacing pulses are applied to the atria and/or the ventricles in response to a detected bradycardia or dissociation of the atrial and ventricular heart rates at a pacing rate to restore cardiac output that is appropriate to the physiologic requirements of the patient. Moreover, anti-tachycardia bursts of pacing pulses or single overdrive pacing pulses are applied to the atria and/or the ventricles to counter and convert certain low rate AT or VT episodes to normal sinus rates. Such pacing pulses have well-defined amplitude and pulse width characteristics which can be adjusted by remote programming and telemetry equipment to meet physiologic needs of the particular patient and device power conservation requirements.
It is known in the ICD art to provide a "tiered" therapy with regard to the termination of sensed tachyarrhythmias. The term "tiered" therapy has been used typically to describe the different tachyarrhythmia rate zones, such as low rate ventricular tachycardia (VT Low), high rate tachycardia (VT High), and VF. The term "tiered therapy" also has been used to describe the increasing degree of aggressiveness within each rate zone. For example, within each zone the physician may program the number and types of therapies to be delivered, the intervals between applied therapies, the energy level of the therapy, etc. Thus, based upon the detected rate of the arrhythmia, the ICD will continue to increase the level of aggressiveness until such arrhythmia is terminated.
Cardioversion is often thought of as being "low energy" since the heart has been known to successfully convert the arrhythmia with electrical shocks in the range of 0.1 to 10 joules. However, it is still classified as cardioversion if the arrhythmia is a ventricular tachycardia even if the energy required to convert the arrhythmia goes up to the maximum value that the ICD is capable of delivering. (e.g., 40 joules). Defibrillation, on the other hand, is often thought of as being "high energy" since the heart has been successfully defibrillated with energy shocks in the range of 11 to 40 joules. In contrast, the pacing pulses that are applied to a heart during normal or anti-tachycardia pacing are typically of much lower energy (e.g., between 50 and 200 micro joules). The principal difference between the types of therapy provided by an ICD supporting tiered therapy is that of arrhythmia detection and the programmed level of aggressiveness with the therapy typically starting by applying the lowest energy stimulation for that detected arrhythmia and working its way up to high energy shock therapy, as required.
To detect and classify tachyarrhythmias, one or two basic strategies are generally followed which start with identifying atrial and/or ventricular sensed events and deriving atrial and/or ventricular event intervals and/or rates therefrom. The event intervals are compared to programmed fibrillation detection interval ranges and tachycardia detection interval ranges and to suddenness of onset criteria and rate variability criteria to distinguish various tachyarrhythmias from one another. In the first strategy, the event intervals are compared with a preset group of criteria which must be met as precedent to detection or classification. As the episode progresses, the first set of criteria to be met results in detection and diagnosis of the tachyarrhythmia. The second strategy is to define a set of criteria for events, event intervals and/or rates which is generally indicative of a group of arrhythmias; following the satisfaction of those criteria, preceding or subsequent events are analyzed to determine which specific tachyarrhythmia is present. The Model 7219 ICD commercially available from Medtronic, Inc., employ an arrhythmia detection and classification system, generally as disclosed in commonly assigned U.S. Pat. No. 5,342,402, incorporated herein by reference in its entirety, which uses both strategies together. Numerous other or additional detection and classification systems have been proposed as set forth in commonly assigned U.S. Pat. Nos. 5,545,186, 5,782,876, and 5,814,079, incorporated herein by reference in their entireties.
Menus of such tachyarrhythmia detection criteria and anti-tachyarrhythmia therapies that are tailored to a range of detected tachyarrhythmias are typically provided in such current ICDs. The above-incorporated patents and U.S. Pat. Nos. 4,830,006, 4,726,380, and 4,587,970, all incorporated herein by reference in their entireties, illustrate such detection criteria and therapy menus. The particular therapies that are to be provided upon detection of particular tachyarrhythmias in an individual patient are remotely programmed into ICD memory by the physician. For example, upon sensing a low rate AT or VT, an ICD may attempt to terminate such a tachycardia by first applying a prescribed anti-tachycardia pacing therapy to the atria or ventricles, respectively. Such anti-tachycardia pacing therapies typically includes burst pacing, ramp pacing, adaptive pacing and/or scanning pacing, as is known in the art. See, e.g., U.S. Pat. Nos. 4,427,011 and 4,541,430 (burst pacing); 4,398,536 (ramp pacing); and 5,103,822 (scanning pacing); which patents are incorporated herein by reference in their entireties. Upon re-detection of the AT or VT, a more aggressive anti-tachycardia pacing therapy may be scheduled.
If the anti-tachycardia pacing therapy is unsuccessful or inappropriate, the ICD may be programmed to apply a low energy, cardioversion energy shock in an attempt to cardiovert the heart. In order to apply a cardioversion or defibrillation shock to a heart chamber, it is first necessary to charge one or more high voltage (HV) output capacitors of the ICD device with to a voltage providing the programmed energy upon discharge through the cardioversion/defibrillation electrodes. When the HV output capacitors are charged to the programmed voltage, HV output switches are closed to connect the HV output capacitor(s) to the cardioversion/defibrillation electrodes, thereby effectively "dumping" the charge stored in the HV output capacitor(s) across the heart chamber.
The tiered therapy ICDs begin to charge their HV output capacitor(s) following initial detection of a tachyarrhythmia or re-detection of the tachyarrhythmia episode that has not been terminated by a previously delivered less aggressive therapy. For example, if the ICD sensing and logic circuits determine that the first tier cardioversion/defibrillation therapy has not successfully terminated the tachyarrhythmia, the HV output capacitors are charged to the appropriate energy for a second tier cardioversion/defibrillation therapy at a higher energy level. As soon as the ICD sensing and logic circuits determine that the second tier cardioversion/defibrillation therapy has not successfully terminated the tachyarrhythmia, the HV output capacitors are charged to a still higher energy level. Unfortunately, it may take 3-4 seconds to charge the high voltage output capacitors to a moderate energy level to (1 to 10 joules), and 7-15 seconds to charge such capacitors to a high energy level (11 to 40 joules). Disadvantageously, these charging times represent a significant period of time, or "time-to-therapy," during which the tachyarrhythmia continues without the benefit of having the ICD apply any therapy.
Considerable effort has been expended in devising efficacious cardiac stimulation and/or shock waveforms and cardioversion/defibrillation electrodes and pathways through the heart in the effort to achieve cardioversion or defibrillation at low energy levels and with shorter charging times. This has been particularly of interest for treating frequently recurring tachyarrhythmias, since the battery life of the ICD depends on the amount of energy expended in delivering a therapy and the delivery frequency.
As noted above, numerous first tier anti-tachycardia pacing therapies have been developed to respond to a given high rate AT or VT preceding delivery of a cardioversion shock in the hope that the low energy pacing pulses would terminate the tachycardia without having to resort to higher energy cardioversion therapies. Or, the low energy pacing pulses have been applied to the heart chamber in the attempt to pre-condition the heart mass to be cardioverted or defibrillated at a lower shock energy. For example, commonly assigned U.S. Pat. No. 5,713,924, incorporated herein by reference discloses delivery of a burst of pacing pulses into a low current density region of the heart chamber prior to and during delivery of a cardioversion/defibrillation shock to that chamber. And, the above-incorporated '079 patent discloses sub-threshold anodal stimulation pulse trains triggered in timed synchronization with a sensed event to a wide area of a heart chamber that is beating at a tachycardia rate to effect maximal cardiac relaxation and to suppress aberrant electrical activity attendant to the sensed cardiac depolarization.
Also, it is known to deliver a pacing pulse following charge up of the HV output capacitors to the heart chamber in the attempt to capture the heart chamber or to make its depolarization more regular to provide the synchronization window for delivery of the cardioversion shock during a refractory period following the delivered pacing pulse. In a further U.S. Pat. No. 5,074,301, a ventricular tachyarrhythmia detection and cardioversion system is disclosed wherein it is proposed to deliver a pacing pulse to the atrium prior to delivery of a cardioversion shock to the ventricle in VT to reduce the possibility that the delivered cardioversion shock would trigger a post-shock atrial arrhythmia. The atrial pacing pulse captures the atrium and renders it refractory, and the ventricular cardioversion shock is delivered during the atrial refractory period.
Hemodynamic collapse is a common condition that occurs during ventricular tachyarrhythmia, particularly in patients having depressed ventricular function. It's severity depends on the rate of the tachyarrhythmia as well as on the responsiveness of the patient's neurally mediated compensatory mechanisms. With drop in blood pressure, arterial baroreceptors invoke a sympathetic vasoconstrictor response to increase peripheral resistance and maintain pressure. Previous work reported by Hamer et al., entitled "Hemodynamic Benefits of Synchronized 1:1 Atrial Pacing During Sustained Ventricular Tachycardia With Severely Depressed Ventricular Function in Coronary Heart Disease" (Am. J. Cardiol., 1985, vol. 55, no. 8,990-94), suggests that this neural reflex may be offset by an opposing reflex involving pressure (or stretch) receptors in the atria. Atrio-ventricular dysynchrony during VT can result in coincident atrial and ventricular contractions which not only results in reversal of blood flow into the veins entering the heart, but also may result in atrial stretch and activation of a vasodilating reflex.
A recent abstract by Wong et al., entitled "Sinus Node Behavior During Stable and Unstable Ventricular Tachycardia with Ventricular-Atrial Dissociation" (JACC Abstracts, February 1999, 1204-185), demonstrates the importance of neural reflexes in mitigating hemodynamic collapse during VT. Wong et al. observed that stable VT was characterized by sinus node acceleration whereas unstable VT was not. This work suggests that autonomic modulation of blood pressure does play a role in maintaining blood pressure during VT.
Hemodynamic collapse during unstable ventricular tachyarrhythmias can occur during the initial and succeeding HV charging times if successive, same or tiered therapies are necessary as described above. Although ICDs have been shown to be highly effective in aborting sudden death from malignant ventricular tachyarrhythmias, their ability to prevent syncope or incapacitating pre-syncopal prodromes are limited. This is particularly the case due to the above-described charging time that it takes to charge the HV output capacitors to the prescribed voltage to deliver a cardioversion shock therapy. As a result, ICD patients are advised to significantly curtail or refrain completely from activities that put themselves or others at risk, such as driving a vehicle, operating other equipment, swimming in open water, riding a bicycle, or others that cannot accommodate near or complete loss of consciousness for only a few seconds. For many patients, necessary sacrifices for the sake of safety not only take away their ability to continue to be productive in their professional and in their private lives, but they also restrict their ability to participate in many of life's simple pleasures.
A need exists to avoid or alleviate such hemodynamic collapse following the onset of an unstable VT episode and until an anti-tachycardia cardioversion/defibrillation shock is delivered that successfully converts the ventricles back to normal sinus rhythm.